Boissard Romuald, Fort Patrice, Gervasoni Damien, Barbagli Bruno, Luppi Pierre-Hervé
CNRS UMR5167, Institut Fédératif des Neurosciences de Lyon (IFR 19), Université Claude Bernard Lyon I, 7, Rue Guillaume Paradin, 69372 Lyon, Cedex 08, France.
Eur J Neurosci. 2003 Sep;18(6):1627-39. doi: 10.1046/j.1460-9568.2003.02861.x.
We recently determined in rats that iontophoretic application of bicuculline or gabazine [two GABAa antagonists] and kainic acid (a glutamate agonist) in the sublaterodorsal nucleus (SLD) induces with a very short latency a paradoxical sleep-like state. From these results, we proposed that GABAergic and glutamatergic inputs to the SLD paradoxical sleep (PS)-executive neurons gate the onset of PS [R. Boissard et al. (2002) Eur. J. Neurosci., 16, 1959-1973]. We therefore decided to determine the origin of the GABAergic and non-GABAergic inputs to the SLD combining ejection of a retrograde tracer [cholera-toxin B subunit (CTb)] with glutamate decarboxylase (GAD) immunohistochemistry. The presence of GAD-immunoreactive neurons in the SLD was confirmed. Then, following CTb ejections centred on the SLD, combined with GAD and CTb immunohistochemistry, double-labelled cells were observed in the mesencephalic and pontine reticular nuclei and to a lesser extent the parvicellular reticular nucleus. A large number of GAD-negative retrogradely labelled cells was also seen in these structures as well as in the primary motor area of the frontal cortex, the central nucleus of the amygdala, the ventral and lateral bed nucleus of the stria terminalis, the lateral hypothalamic area, the lateral and ventrolateral periaqueductal grey and the lateral paragigantocellular reticular nucleus. From these results, we propose that the activation of PS-executive neurons from the SLD is due to the removal of a tonic inhibition from GABAergic neurons localized in the SLD, and the mesencephalic and pontine reticular nuclei. Strong non-GABAergic inputs to the SLD could be excitatory and responsible for the tonic glutamatergic input on the PS-on neurons we have previously described. They could also terminate on SLD GABAergic interneurons and be indirectly responsible for the inhibition of the PS-on neurons during waking and slow-wave sleep.
我们最近在大鼠中确定，在外侧背核（SLD）中离子电渗法应用荷包牡丹碱或加巴嗪[两种GABAa拮抗剂]和 kainic 酸（一种谷氨酸激动剂）会在非常短的潜伏期内诱导出一种类似异相睡眠的状态。基于这些结果，我们提出，向SLD异相睡眠（PS）执行神经元的GABA能和谷氨酸能输入控制着PS的起始[R. Boissard等人（2002年），《欧洲神经科学杂志》，16，1959 - 1973]。因此，我们决定结合逆行示踪剂[霍乱毒素B亚基（CTb）]的注射与谷氨酸脱羧酶（GAD）免疫组织化学来确定向SLD的GABA能和非GABA能输入的来源。SLD中GAD免疫反应性神经元的存在得到了证实。然后，在以SLD为中心进行CTb注射后，结合GAD和CTb免疫组织化学，在中脑和脑桥网状核以及较小程度上在小细胞网状核中观察到了双标记细胞。在这些结构以及额叶皮质的初级运动区、杏仁核的中央核、终纹床核的腹侧和外侧、外侧下丘脑区、外侧和腹外侧导水管周围灰质以及外侧巨细胞旁网状核中也看到了大量GAD阴性的逆行标记细胞。基于这些结果，我们提出，来自SLD的PS执行神经元的激活是由于位于SLD以及中脑和脑桥网状核中的GABA能神经元的紧张性抑制被解除。向SLD的强大非GABA能输入可能是兴奋性的，并对我们之前描述的PS开启神经元上的紧张性谷氨酸能输入负责。它们也可能终止于SLD的GABA能中间神经元，并间接负责在清醒和慢波睡眠期间对PS开启神经元的抑制。
